No abstract

We herein show a case of symptomatic common carotid artery occlusion that underwent bonnet bypass (contralateral superficial temporal artery (STA) -saphenous vein (SV) -cortical segment (M4) of the middle cerebral artery (MCA) bypass) using an SV graft. STA-MCA bypass surgery has been established for the prevention of secondary cerebral infarction of symptomatic internal carotid artery occlusion. On the other hand, there has been no standard surgical treatment for symptomatic common carotid artery occlusion. It has been reported that bonnet bypass using donor grafts is effective for these pathological conditions. We herein performed bonnet bypass surgery using an SV graft as a donor graft. The vascular reserve was improved in quantitative single photon emission computed tomography, the bypass patency was also spared, and the postoperative course was uneventful.

Background: High mobility group box 1 (HMGB1) is a chromatin structural protein expressed ubiquitously in the nuclei of mammalian cells. Increasing evidence suggests that inflammatory responses are involved in the progression of systemic injuries induced by a diverse range of insults, including stroke, trauma, tumors, and degenerative diseases. Whether HMGB1 expression in systemic organs is associated with transient ischemic attack (TIA) remains unclear. We hypothesized that HMGB1 expression after TIA would exacerbate systemic symptoms due to acute inflammation.Material and Methods: We performed transient bilateral and unilateral common carotid artery occlusion (2VO and 1VO) on Sprague-Dawley (SD) male rats. Rats were randomized to the sham, 1VO, and 2VO groups. The sham group underwent no procedure that involved common carotid artery occlusion. Common carotid arteries were clamped for 30 minutes and, subsequently, reperfused for 24 hours. Brain, heart, liver, lung, spleen, kidney and intestine tissue samples were collected for biochemical and histopathological analysis. Protein and mRNA expression were determined by western blot analysis and polymerase chain reaction (PCR).Results: HMGB1 expression increased in the brain, liver, spleen and intestine of the rat 1VO and 2VO models. In vivo results indicated high expression of HMGB1 in TIA, and the expression of MMP-9 and PKCδ in the cerebral cortex and hippocampus was regulated by HMGB1. In the 2VO model, the expression of CD11b and GFAP in the cerebral cortex was significantly increased compared with that in the control group (P < 0.001). HMGB1 was translocated from the nucleus to the cytoplasm at early stages after TIA and then localized to the cytoplasm of phagocytic microglia at later stages.Conclusion: HMGB1 expression increased in the systemic organs after TIA. HMGB1 promotes systemic inflammation, which mediates the immune response and tissue damage in the brain after TIA. Targeting HMGB1 signaling may be a promising therapeutic approach for the treatment of TIA.